Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model.
The role of the pancreaticotrophic hormone cholecystokinin (CCK) in modifying the pancreatic response to carcinogen has been examined in the hamster-nitrosamine pancreatic cancer model. Exogenous CCK, 30 IDU kg-1, stimulated a maximal pancreatic secretory response when given intravenously and caused...
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| Format: | Online |
| Language: | English |
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1985
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1976814/ |
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pubmed-1976814 |
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pubmed-19768142009-09-10 Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. Howatson, A. G. Carter, D. C. Research Article The role of the pancreaticotrophic hormone cholecystokinin (CCK) in modifying the pancreatic response to carcinogen has been examined in the hamster-nitrosamine pancreatic cancer model. Exogenous CCK, 30 IDU kg-1, stimulated a maximal pancreatic secretory response when given intravenously and caused hypertrophy and hyperplasia of the pancreas when given subcutaneously over a period of 6 weeks (pancreatic wet weight, mg per 100 g body weight, controls 295.6 +/- 61; CCK treated 466.4 +/- 77, P less than 0.001). When the same dose of CCK was given to animals receiving N-nitrosobis (2-oxopropyl)amine (BOP; 5 mg kg-1 weekly) there was a reduction in latency period and increase in induction rate of tumour development (CCK + BOP vs. BOP alone, 12 animals with tumours vs. 2 at 15 weeks; P less than 0.02). These effects are consistent with CCK acting as a co-carcinogen or promoter of pancreatic carcinogenesis in this model. 1985-01 /pmc/articles/PMC1976814/ /pubmed/3966964 Text en |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Howatson, A. G. Carter, D. C. |
| spellingShingle |
Howatson, A. G. Carter, D. C. Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. |
| author_facet |
Howatson, A. G. Carter, D. C. |
| author_sort |
Howatson, A. G. |
| title |
Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. |
| title_short |
Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. |
| title_full |
Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. |
| title_fullStr |
Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. |
| title_full_unstemmed |
Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. |
| title_sort |
pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model. |
| description |
The role of the pancreaticotrophic hormone cholecystokinin (CCK) in modifying the pancreatic response to carcinogen has been examined in the hamster-nitrosamine pancreatic cancer model. Exogenous CCK, 30 IDU kg-1, stimulated a maximal pancreatic secretory response when given intravenously and caused hypertrophy and hyperplasia of the pancreas when given subcutaneously over a period of 6 weeks (pancreatic wet weight, mg per 100 g body weight, controls 295.6 +/- 61; CCK treated 466.4 +/- 77, P less than 0.001). When the same dose of CCK was given to animals receiving N-nitrosobis (2-oxopropyl)amine (BOP; 5 mg kg-1 weekly) there was a reduction in latency period and increase in induction rate of tumour development (CCK + BOP vs. BOP alone, 12 animals with tumours vs. 2 at 15 weeks; P less than 0.02). These effects are consistent with CCK acting as a co-carcinogen or promoter of pancreatic carcinogenesis in this model. |
| publishDate |
1985 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1976814/ |
| _version_ |
1611400630511861760 |